Ventyx Biosciences Q1 2024 Earnings Call Transcript

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May 9, 2024

There are 6 speakers on the call.

Operator

Good afternoon, ladies and gentlemen, and welcome to the Fintix Biosciences First Quarter 2024 Earnings Conference Call. At this time, all parties have been placed in a listen only mode and the floor will be open for your questions following the presentation. As a reminder, this conference call is being recorded. I would now like to turn the call over to Doctor. Marty Oster, Ventex' Chief Financial Officer.

Operator

Please begin.

Speaker 1

Thank you, operator, and good afternoon to everyone joining us today. Welcome to Ventex Biosciences conference call and webcast, where we'll be discussing our Q1 2024 financial results and providing a corporate update. Before we begin, I would like to remind everyone that today's presentations will include forward looking statements. These statements are subject to risks and uncertainties that may cause actual results to differ materially from those projected. A description of these risks can be found in our Form 10 Q for the quarter ended March 31, 2024, which was just recently filed this afternoon.

Speaker 1

Any forward looking statements are made only as of today's date, and we assume no obligation to update any forward looking statements made on today's call. With that, I'll hand the call over now to Doctor. Raju Mohan, Ventyx's Founder and CEO. Raju, please go ahead.

Speaker 2

Yes. Thanks, Marty, and thank you everyone for joining us our Q1 2024 earnings call and corporate update. As we recently provided a full pipeline and strategic update at our March Investor Day, I will be brief with my remarks today. Let me take a few minutes to provide some high level comments on the status of our pipeline programs, and then I'll hand the call back to Marty to review our Q1 financial results. We'll then open the floor to Q and A, where I'll be again joined by Marty and also with John Nuss, our Chief Scientific Officer.

Speaker 2

So I'll begin with our portfolio of potential best in class NNRP3 inhibitors. In March, we announced positive top line results from a Phase 1 single and multiple ascending dose trial of PTX-three thousand two hundred and thirty two, our novel CNS penetrant NLRP3 inhibitor in adult healthy volunteers. As you may remember, repeat BTX-three thousand two hundred and thirty two doses as low as 3 milligrams once daily achieved steady state IL-one beta IC50 coverage in both plasma and the CSF and repeat doses of 20 milligrams all the way up to 40 milligrams QD will exceed IL-one beta IC90 coverage in both plasma and CSF. Based on these data and our on a dose projection modeling, we estimate that PTX-three thousand two hundred and thirty two doses as low as 12 milligram once daily may be adequate to achieve IL-one beta IC90 target coverage in the CSF and in plasma. We also observed robust dose dependent pharmacodynamic or PD effects in a whole blood ex vivo IL-one beta stimulation assay.

Speaker 2

And VTX-three thousand two hundred and thirty two also showed excellent tolerability profile in this Phase I study. We thus believe that these data establish VTX-three thousand two hundred and thirty two as a potential best in class drug candidate for the treatment of neuro inflammatory diseases

Operator

and conditions.

Speaker 2

This includes excellent target coverage in plasma and CSF, favorable safety profile and a convenient once daily oral regimen with our tablet formulation. VTX-three thousand two hundred and thirty two is a Phase 2 ready compound. As we also communicated in March, we plan to rapidly advance VTX-three thousand two hundred and thirty two into Phase 2 trials in high value indications with substantial unmet need, beginning with the Phase 2a trial of VTX-three thousand two hundred and thirty two in patients with early Parkinson's disease, which we will initiate in the second half of this year. As we discussed, a growing body of preclinical evidence has implicated NLRP-three mediated information as a key driver of Parkinson's disease pathology by impacting neuronal death and degeneration. We therefore believe that NLRP3 inhibition represents a promising, potentially disease modifying therapeutic approach in this devastating neurodegenerative condition.

Speaker 2

More recently, NNRP3 has also created much buzz and discussion as a potentially important target for obesity and obesity related metabolic diseases, much of it due to data published last February showing central NLRP3 mediated weight loss in obese mice. We have initiated our own studies with VTX-three thousand two hundred and thirty two and Neurine models of diet induced obesity similar to the published model we just talked about. In addition to assessing weight loss induced by VTX3,232 and with the GLP-one agonist, semaglutide, In a monotherapy study, we're also evaluating VATX-three thousand two hundred and thirty two in combination with samaglutide. These are exciting studies and we look forward to providing an update on these studies later in the Q2. So now moving from mice to humans, we plan to initiate a Phase 2 trial of VTX-three thousand two hundred and thirty two during the second half of twenty twenty four in obese participants with certain additional cardiovascular risk factors.

Speaker 2

Now moving on to our vtx2735, our peripherally restricted NRRP3 inhibitor. In March, we announced positive top line results from our Phase 2 trial of BTX-two thousand seven hundred and thirty five in patients with cryoprin associated periodic syndromes or CAPS. In this trial, VTX-two thousand seven hundred and thirty five demonstrated efficacy comparable to that observed with IL-one biologics, the current standard of care. VTX-two thousand seven hundred and thirty five also demonstrated consistent robust reductions in inflammatory biomarkers such as HCF CRP, high sensitive CRP, IL-six, serum amyloid A and fibrinogen. There was also a mean reduction of 85% the key symptom score for these GAPS patients during the initial treatment period with a very favorable safety profile with all treatment related adverse events graded as mild.

Speaker 2

These Phase 2 data in CAS patients is therefore a compelling proof of mechanism for VTX2735 for our peripheral inhibitor and for systemic inhibition of NLRP3 and NLRP3 related biomarkers in general, including HSCRP and IL-six. And as we communicated in March, we plan to evaluate VTX2735 for future development and cardiovascular and potentially other indications with an initial focus on recurrent pericarditis and also in the secondary prevention of major adverse cardiovascular events or MACE. Both recurrent pericarditis or RP and MACE prevention represent indication with large addressable markets and substantial unmet medical need. So we thus plan to update or provide an update on our cardiovascular development plans later in this year. Beyond our NNR P3 inhibitor portfolio, the team continues to make progress advancing our IBD assets, including VTX-two, our potential best in class S1P1 receptor modulator for ulcerative colitis and VTX-nine fifty eight, our Allosteric T2 inhibitor in Phase 2 development for the treatment of Crohn's disease.

Speaker 2

For VTX-two, you recall that we announced positive Phase 2 data in October of 2023, demonstrating what we believe is a potential best in disease profile for an oral agent in ulcerative colitis. This includes a highly differentiated rate of complete endoscopic remission and a potential best in class safety profile. At the March event, we also showed preliminary data from the open label extension part of the Phase II trial, further reinforcing the endoscopic remission data and the differentiated profile. We anticipate that the data from the 52 week long term extension part of this Phase 2 study will continue to show sustained or perhaps even improved data for endoscopic remission from that observed in the 13 week induction period. This program is fully Phase 3 ready and our teams continue to make preparations for a pivotal Phase 3 trial is ongoing.

Speaker 2

Last month, we completed a productive end of Phase 2 meeting with the FDA and we expect to conduct a scientific advice meeting with the EMA later this quarter. We continue to have confidence that our completed Phase 2 trial may be sufficient to support approval of VTX-two with successful completion of a second pivotal 52 week trial in ulcerative colitis. And as we have previously indicated, efforts are underway to identify a partner or other source of non dilutive financing to support this pivotal Phase III trial. Finally, our Phase II trial of VTX-nine fifty eight, our allosteric TIG2 inhibitor in moderately to severe active Crohn's disease continues to progress. As we've mentioned, in the Q1 of this year, we implemented a protocol amendment to streamline detection of a potential efficacy signal in this trial.

Speaker 2

As a result of the protocol amendment, target enrollment was revised from approximately 132 patients to approximately 93 patients. And the trial's sole primary endpoint is now the change from baseline in the main Crohn's disease activity index or CDAI score at week 12. We have completed enrollment in the trial in March and we look forward to reporting top line results in early second half of twenty twenty four. So in conclusion, I would like to again thank all of Aventics' team members for their continued efforts and contributions across the pipeline to our investigators and collaborators and of course all the patients that enroll in our trials. We are very much looking forward to a productive year for VENTIX and to continue to provide these exciting updates.

Speaker 2

I'll now hand the call back to Marty for a brief review of our financial of our Q1 financial results.

Speaker 1

Marty? Yes. Thank you, Raju. Our financial results for the Q1 ended March 31, 2024 are point $7,000,000 compared to $35,400,000 in the Q1

Speaker 2

of 2023. G and A expenses

Speaker 1

in the Q1 of 'twenty four were $8,000,000 compared to $7,100,000 for the Q1 of 2023 and our net loss in the Q1 of 2024 was $38,600,000 compared to a $38,900,000 net loss in the Q1 of 2023. Our cash, cash equivalents marketable securities balance was $302,600,000 as of March 31, 2024. Net cash used in operating activities during the Q1 of $47,600,000 was higher than the reported operating expenses of $41,800,000 and is primarily due to an increase in prepaid expenses and a decrease in accrued expenses during the quarter. We expect both our operating expenses and our operating cash flows on a quarterly basis to decrease we get into Q2 of 2024 and remain lower for the rest of 2024 as we complete the wind down activities related to our Phase 2 trial programs in psoriatic arthritis for VTX-nine fifty eight. We continue to believe that our current cash, cash equivalents and marketable securities are sufficient to support our planned operations into at least the second half of twenty twenty six.

Speaker 1

This concludes our prepared remarks for this afternoon's call, and I'll now turn the call back to the operator to begin the Q and A session. On the Q and A session, I'll be joined by Doctor. Rajeev Mohan as well as our Chief Scientific Officer, John Noss. Operator, please go ahead.

Operator

First question comes from Michael Yee with Jefferies.

Speaker 3

Hey guys, thanks for the question. This is Kyle for Michael. So on the CNS penetrant NLRP3 program, what do you think is promising for a 28 day study in human or oral like this? And what do you think is the bar? And how do you think it stacks up other injectables and oral options under investigation?

Speaker 3

And a quick one on your mouse data, where do you think you're going to present the data? Is it going to be in the format of a press release? Or are you going to report it at a conference? Thank you.

Speaker 2

Well, thanks. So let me address the second question first. So we will as I mentioned before, we plan to report this data in the late second quarter. And we're in the process of compiling the data. And once we have all that together, we'll decide what the right forum for presenting it.

Speaker 2

So just stay tuned. In terms of your questions about sort of what we expect to see in 28 days, I think there's plenty of studies out there, not just with GLP-one agonist, but other modalities as well, showing measurable weight loss in 28 days in human trials, anywhere from single digits, 2% higher weight loss. So again, it remains to be seen what the competitor data will show if and when the data are put out. In our mind, we have 2 things happening. 1 is obviously we've done we're repeating the study that was published in diet induced obese mice.

Speaker 2

As we mentioned, it's a monotherapy study with compound in a control and it's a combination study with semaglutide and we're looking forward to reporting these results. We also, as we've said, committed to doing our own trial, 20 day trial in patients and we think there's biology out there now that certainly links NRP3, NRP3 activation or inhibition to hypothalamic control of obesity parameters or mechanisms such as feeding behavior. And I think that that body of evidence will continue to grow as folks try to link the dots just like it's been happening for Parkinson's disease. So, we're committed to doing this trial. We look forward to seeing the data from the competitor if and when it's put out there.

Speaker 2

But our own path here is planned, which is again, put out the mouse data and then filing for our Phase 2a study in obese patients latter half of the year. All right. Thanks.

Operator

Thank you. Our next question comes from Yasmeen Rahimi with Piper Sandler.

Speaker 4

Hi. This is Liam Hester on for Yas. So, I guess my first question is related to what's the current talk package available for VTX3,232? And then when moving on to the expected Phase 2 trial, what work still needs to be done in order to initiate in obese patients with additional CV risk? And then moving to 2,735 with those Phase II trials, what are the rate limiting steps in initiating a MACE or a current pericarditis trial there?

Speaker 2

All right. So let me start with the first one. So our first study is a 28 day study. These patients, it's a similar study we are planning, a 28 day study in early Parkinson's disease. And then we will initiate the longer term studies, particular the obesity study if that merits the Phase 2 in the latter half of the year.

Speaker 2

So right now on the TOX packet, we'll support a 28 day study and then we'll have the TOX coverage to do chronic studies in the latter half of the year. 2nd question was on briefly, if you don't mind repeating the second one.

Speaker 4

Yes. So I guess like for the 2,70035 asset, what are the rate limiting steps for the initiation of the Phase 2 MACE trials and pericarditis?

Speaker 2

There's no rig. Every trial has to have its own individual planning. The teams have to get together, the protocols have to be written and the contracting has to be done. We've laid out our timelines for the Parkinson Obesity trial and we lay out the timelines for the cardiovascular trials once those have been firmed up, there's still rate limiting stuff. It's just a part of the planning process on going from a Phase I study to a Phase II study.

Speaker 2

So it's just standard process that we have here. But we're pretty excited about the cardiovascular opportunities for 2,735, both in recurrent

Speaker 4

VTX002, just wondering if you could provide like any more detail on the level of partnership interest? And then also any details from the end of Phase 2 meeting?

Speaker 2

Yes. So on the end of Phase 2 meeting, we had a really good meeting with the FDA and we laid our justification for a Phase 3 trial with a single dose and we believe this we believe this should serve as a pivotal trial as should the first one. And we'll have continue to have those discussions with agency as the trial progresses. So, our mind is very successful meeting with the FDA. In terms of partnerships, we're not going to get into specifics.

Speaker 2

We think this compound continues to show a very strong endoscopic remission as we showed from the open label. We believe the long term extension data will continue to support both the durability of this and perhaps even improved scores, such as the precedent with S1P1 modulators. And as we said, we are aggressively in the midst of getting interest from pharma partners across a wide range of folks. And stay tuned and we'll update you guys once those things progress to something that we can talk about.

Operator

Thank you. Our next question comes from Emily Bodner with H. C. Wainwright.

Speaker 5

Hi. Thanks for taking the question. For Parkinson's disease, I'm curious if you can comment on what kind of neurodegenerative markers you're planning to evaluate and if you're looking at any disease rating scores or kind of impacts on motor symptoms. And maybe if you could provide a bit more on study design for obesity in terms of like how many patients you're planning to evaluate? And are you planning to exclude diabetes patients in that study?

Speaker 5

Thanks.

Speaker 2

Yes. Good questions. So, again, on specific of the trial and we're not trying to be KG. We don't necessarily disclose every aspect of this trial. Once we have it, it will be on clinicaltrials.gov.

Speaker 2

But again, just to bring it in context, you saw the competitors' 28 day trial within an RP3 compound a few months back. They published a biomarker trial. We are planning not just a biomarker trial, but we also have an imaging component to this trial to see effects of this molecule on glial content and activation as it translates into eventual effects on astrocytes and eventually neural death. Don't expect much effect on motor symptoms in these short trials, but we certainly expect to see effects on, number 1, the LNRP3 related biomarkers such as IL-one beta, HSCRP, IL-six, Rabinogen, we've shown them now convincingly in multiple trials. Even in early Phase 1, We've seen some movement in these trials in these markers, even in healthy volunteers.

Speaker 2

We certainly showed a robust response of an NLRP3 compound, albeit the peripheral one in HFCRP and again IL-one beta and IL-six. And then the Phase I trial with 3,232, we also showed effects on these biomarkers even in healthy volunteers and in the CSF, right? So those are NLRP 3 rated biomarkers. And then you have the other side of neurodegenerative markers, in particular with Parkinson's patients such as neurofilament light chain and others. And again, thoughtfully explore a range of biomarkers.

Speaker 2

There is nothing that precludes us from having a much broader set in our measuring strategy. But again, we're not setting any expectation of seeing any sort of meaningful effects of the SHORT trial and that's why we have a longer trial that we are contemplating towards the end

Speaker 1

of the year, which will be

Speaker 2

much more in line with what you've seen recently or published for much longer treatment in Parkinson's patients. And these are 12 months or longer trials.

Speaker 5

Okay. Makes sense. Thank you.

Operator

Thank you. We will take our next question from Vikram Parohit with Morgan Stanley.

Speaker 2

Hi, everyone. This is Gaspar on for Vikram. We have one question regarding your CD program. What is the hurdle for continuing VTX-nine fifty eight in Crohn's disease based on the data expected in the second half of the year? Yes.

Speaker 2

Thanks, Vikram. And perhaps I'll let Marty address this. Marty?

Speaker 1

Yes. Thanks for the question, Gonsal. So for that trial, the primary endpoint is a change in CDI score and then we're looking at key secondary endpoints that include like endoscopic response and things like that. If you look across sort of approved drugs in the Crohn's disease space, you're looking at some of the biologics as well as more recent developed products like upadacitinib. You'll see CDI changes in the Phase 2 in the range of the upper double digits to kind of low 100 as sort of a kind of a meaningful type of response on that marker.

Speaker 1

We're adequately powered to sort of detect statistical significance that type of response. And then on the endoscopic side, that's a secondary endpoint given the size of the trial, But we'd be looking to see sort of again something competitive there would be in the high teens to low 20s endoscopic response versus relative delta versus placebo. That's sort of kind of I think where the bar is for recently proved drugs to be attractive in this setting. So we're looking forward to reporting those results out to you in the next several months.

Speaker 2

Thank you very much.

Operator

Thank you. We will take our next question from Alex Thompson with Stifel.

Speaker 3

Hey, great. Thanks for taking my questions. I guess first one on 3,232 to follow-up a little bit on the DIO mouse experiment. Can you talk a little bit about sort of the human dose equivalents you're going

Speaker 4

to be testing relative to what you're looking for

Speaker 3

on the Phase 2 and what you want to see in both the monotherapy and combo studies to get more confident in the human trial? And then for 2,735, just curious your thoughts on peripheral NRP 3 inhibition in the context of what we saw from ludukizumab at AAD and whether you would consider an indication like HS in the future? Thanks.

Speaker 2

Yes. So first on human dose equivalent in the mouse study. So the mouse we don't do these studies in rodents, whether it's for an RRP-three or anything else. It's really a proof of concept and you appropriately dose the animals based on the profile of the compound in mice, for example, right? So the exposure in mice, the potency of the compound in, for example, against mouse NLRB3.

Speaker 2

And that's the goal. It's not to determine the human dose. Remember, we've done a Phase 1 trial with biomarkers in plasma and in CSF. We've calibrated that trial with what we expect to have the exposure to cover IL-one beta IC50, IL-one beta ID90. And if IL-one beta is the driver or IL-eighteen, but IL-one beta and IL-eighteen are the drivers of the disease pathology.

Speaker 2

So that's the calibration. So what doses do we need in humans to have complete aggregation or complete inhibition of the IL-one beta produced by NLRB3 in periphery or in the CNS and the CSF is a good surrogate. So just to make it clear, the mouse studies are not meant to find doses for the obesity trial or Parkinson's trial or any other Phase 2 trial. So in terms of mice, again, the doses are now set to make sure that we have adequate coverage in the mice to see effects on weight loss, to see effects on other endpoints and it again depends on the compound. So we don't take any sort of guidelines from the competitor dosing paradigm, in which case it was 3 times a day in mice.

Speaker 2

We have our own dosing regimen and that's what we've done in both trials, the monotherapy and the combo therapy. I think the expectation that you have the question you had is what do we expect to see in a combination trial. First of all, we this whole trial the old study, I shouldn't call it a trial, in mice was really to have our own calibration of our compound, which is a really well behaved CNS drug, I think the best behaved CNS phenocrine compound out there in the NLRP3 class. And so our goal is to set our own calibration in terms of these mice models, which we believe are in different parameters predictive of human disease. So it's not a one to one mouse model as a human model.

Speaker 2

It's different aspects and different readouts from this study recapitulate what you expect in human studies, right, in this case obesity. So having no expectation, but having the competitive data, we designed this trial with a compound, with the semaglutide control and with adequate controls with a placebo. First thing to see whether you see any weight loss. Would our compound obviously have weight loss from somaglutide that's been published many times as it's published in the competitor compound data that you saw. Next thing is to understand effect of weight loss, effect of food intake And then once the study is completed, what happens to other parameters, lipid parameters, what happens to diabetes parameters like glucose, insulin, OGTT, HOMA IR, what's happening to steatosis.

Speaker 2

So as we know, obesity or reduction in obesity results in benefit on a number of parameters, so we look for that. In the combo study, obviously, we would look for not just effects of monotherapy, but what is the effect of anonarky 3 inhibition on weight loss visavisemantle type alone or a GLP agonist agonist alone? Is it additive? Is it synergistic? Eventually, we'd like to understand that this mechanism is orthogonal.

Speaker 2

So again, this is the mouse studies are really a way to build like the in vitro studies a lot of links in understanding this pathway. So we've done some work in the microglial cells. We'll get data from the mouse studies. And then obviously, we're committed to doing the human study. But it's a pretty exciting stage in this part of the NLRP-three pathway.

Speaker 1

So I've

Speaker 2

always been interested in Parkinson's, but this has opened a whole new area and I think we're sort of in the forefront of this with our molecule to be able to sort of connect the dots. And looking forward to sharing the mouse data with you guys in a few weeks, end of Q2. I think your third question was?

Speaker 1

Potential for 2,755 in HS.

Speaker 2

Potential for 2,755 in HS. Yes, so we think there's potential clear potential for a 2,735 mechanism in HS. I just caution you that the results from the AbbVie study were very, very encouraging. But there isn't a real one to one correspondence between a IL-one beta antibody such as canakinumab and an RP3 mechanism versus the AbbVie, it's an IL-one alpha beta antibody as well as for example, a IL-one alpha beta trap such as rilumab. Right?

Speaker 2

So there's a little bit of an area there that has to be explored. But yes, certainly there is enough rationale for looking at analog PT molecule in HS.

Operator

Thank you. We will take our next question from Derek Archila with Wells Fargo.

Speaker 3

Hi there. Thanks for taking our questions. I guess a couple on TUHIP2. Given what you've seen in your Phase 1 data in the ORTHEREA's NT796 positive outcome in their Phase 1b2a, you think getting to Phase 2b trial is now derisked? And then also do you expect 32, 32 to differentiate from MT-seven ninety six in Parkinson's field?

Speaker 2

Yes. So if I sorry, you were fading out a little bit. So your question was, has the data from Natera in their Parkinson's Phase 2a derisked our trial? That was the question? Yes.

Speaker 2

So let me assume that's a question. So it's always good to see it's always good to see data from any drug in the class where there hasn't been a lot of data out there showing effects on biomarkers in this study, right? But again for us, we believe from our Phase 1 study, everything we've seen, this is our extremely well behaved compound. It's suitable for QD dosing at low doses. We expect to have coverage of IC90 doses starting at 10 to 12 milligrams.

Speaker 2

And it's a real clean single order kinetics dosing profile. So we're looking forward to this 28 day study and generate our own data. Like I said, I don't have any doubts that we'll see effects on IL-one beta downstream markers and LRP3, again, IL-one beta IL-six HSCRP. And we'll establish our own biomarker profile both in blood and in CSF with respect to things like neurofilament light chain and other biomarkers as well. Now there was some data from Natera.

Speaker 2

But our compound is so well behaved because we hit the target so hard that we'll have to set our own calibration for the Phase IIa before we go into a longer Phase II study.

Operator

Thank you. We will take our next question from Sam Slutsky with Life Science.

Speaker 3

Hey, good afternoon, everyone. I hopped on a tad lead, so if you answered any of my questions previously, just let me know. On the obesity preclinical study with 3,232, just kind of generally speaking, how similar or different is the methodology to what Nauthera did in their preclinical study? And then do you anticipate that there will be any bigger conclusions that can be drawn from it other than kind of the binary of it looks good or not on weight loss?

Speaker 2

Yes. Good to hear from you, Sam, and happy to repeat the answers for you. I don't think I've never in my 30 years spent so much time talking about my studies, but happy to do so. So there's really no learnings from the mouse study that the competitor did. Again, it was a pretty standard DIO study.

Speaker 2

So you have obese mice. In olden days, you had to generate these mice by feeding them a high fat diet for 15 weeks or longer. Now these are off the shelf. You can buy obese mice, diet induced obese mice. In terms of so we have done these trials before perhaps looking at different endpoints.

Speaker 2

In this case, the primary endpoint obviously is weight loss and look at secondary endpoints as I mentioned before, the effects on liver weight, body weight, body scan. We're also doing DEXA in this study. We look at lipids, we look at the restatosis, we do staining in the liver. So everything that you would want to read out post the weight loss there as well. Really, again, like I said before, you need to look at individual readings from this study to understand how it translates or potentially translates into what you expect in humans.

Speaker 2

It's not a one to one correlation, right? These models are used for a number of things. You'll see them being used for developing drugs for diabetes. They've been used for DP4 inhibitors. They've been used for SGLT2.

Speaker 2

They've been used for GLP-one agonist. Now we're looking at an RP3. So it's really a broad model and you can take individual pieces from this model and then reconstruct what you would want to see in a human study, right? And again, we're excited about not just this model. This model is just a path for us to go into the humans.

Speaker 2

And so we'll complete the models. We'll get you the data in few weeks and then on to the human study. And in the meantime, our biologists are actively trying to link the dots and understanding hypothalamic interaction with NRP3 and effects on downstream. So just try to build a picture.

Speaker 3

Okay. That's helpful. And just real quick on 2,000 735 on the potential prevention of MACE and pericarditis study. As you think about just that landscape, unmet knee current treatment paradigm, where do you see the profile of 2,725 kind of best slotting in?

Speaker 2

Yes. Let me have Marty. We've thought a lot about it. I'll put them articulators for you. Marty?

Speaker 1

Yes. Sure, Sam. So, obviously, there's some evolution in some of the management of cardiovascular disease. And so that will sort of mature over the time course that we're developing 2,735. I think on the recurrent pericarditis side, you have a pretty classic sort of niche orphan indication with limited therapeutic options.

Speaker 1

Currently, ROLANIS that's really your sort of your go to for difficult to manage refractory patients. It's obviously you may be less than perfect for some patients due to its nature as an injectable therapeutic. It's also a very expensive therapeutic. There's some opportunities certainly to, to I think put forth an oral option for patients who are suffering with recurrent pericarditis symptoms. And I think that disease is often managed now with sort of a bit more of a scattered approach without necessarily a lot of consistency in treatment guidelines and people use things like aspirin and steroids and things like that.

Speaker 1

And I think a very nice targeted NLRP3 inhibitor such as 2,735 could play an important role and obviously the clinical pathway is heavily derisked by the success of IL-one driven biologics in the setting. So excited to kind of develop that and find the right slotting for that in the extreme paradigm.

Speaker 2

Got it.

Speaker 3

All right. Thanks, everyone.

Operator

Thank you. We have no further questions at this time. I now turn the presentation back over to Doctor. Raju Mohan for any additional or closing remarks.

Speaker 2

Yes. Thank you, everybody. Thank you to all on the call. So, we thank you for your continued interest in VENTIX. Obviously, a very exciting period for us.

Speaker 2

We look forward to connecting with you on the Investor Conference in the coming months, connecting with you on the MICE data. We're looking forward talking about our efforts with O2 partnerships moving towards the Phase 3 trial and then hopefully reporting on and coming back and reporting on the ongoing Crohn's trial. So a lot to talk about, but again for today, thank you all and thank you to the team.

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